Midterm 1 Study Guide
Midterm 1 Study Guide Natural Science 2
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Natural Science 2
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This 14 page Study Guide was uploaded by Willow Frederick on Sunday October 2, 2016. The Study Guide belongs to Natural Science 2 at New York University taught by Andre Fenton in Fall 2016. Since its upload, it has received 151 views. For similar materials see Brain and Behavior in CORE at New York University.
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Date Created: 10/02/16
MIDTERM 1 REVIEW/ STUDY GUIDE The Neuron Doctrine 1. Neural units: the brain is made up of individual units that contain specialized features such as dendrites/cell body/axon- all different parts of neurons 2. Neurons are cells 3. Neurons are specialized 4. Nerve fibers are outgrowths of nerve cells 5. Neurons contact each other thru specialized junctions 6. Law of dynamic polarization: there is a preferred direction for transmission from cell to cell (dendritecell bodyaxon) a. A neuron is a communicating element- it has an input & an output 7. Unity of transmission: the contact bw 2 cells can be either excitatory or inhibitory, and will always be of the same tyoe for life 8. Dales’ law: the axon terminal releases a single type of transmitter substance (there are exceptions to this law) Biological Levels of Analysis- ‘the circle of being’ Golgi: NEURAL NET THEORY: Golgi thought neurons were physically connected-not individual neurons Ramón y Cajal: neurons come close to each other but are not continuous— o Neurons are independent from each other o Info from neuron to neuron is transmitted from neuron to neuron across tiny gaps (synapses) All neurons have the same 4 functional zones: input, integration, conduction, & output Synapses are composed of: o Presynaptic membrane, postsynaptic membrane, & synaptic cleft (separates pre- & postsynaptic membranes) Henry Molaison (1926-2008)/ Patient H.M.- had terrible epilepsy, w/many seizures a day o Brenda Milner (neuropsychologist) – figured out that the seizures seemed to be coming from the temporal lobe Removed his hippocampus & amygdala – he became completely amnestic- he couldn’t remember anything – you could hold a convo w him, but if he got distracted, he wouldn’t know who you were memory is localized in its function, in the hippocampus What do the rats in Morris’ water maze tell us? Dorsal Hippocampus is crucial for spatial learning & memory o When neocortical control is cut, the rat can still find the platform quickly, but when the hippocampus is cut, the rat swims all around & has a hard time finding the platform Ventral Hippocampus is crucial for anxiety-related behavior o Turning off the ventral hippocampus makes the rat really brave, & not anxious Are brain functions localized or distributed? –mostly localized Water is polar aka is charged- the charge distribution on the molecule is not balanced, bc physically where the charges exist on a water molecule that on the O there are more e- than on the H side. O is greedy for electrons, so pulls them away from H atoms. O ends up a little more negative and H a little more positivethat’s how water is polar. (O2 is not polar) Measuring the Resting (Transmembrane) Potential o Energy has the capability to do work—to apply a force across a distance o Energy is stored across the membrane that has the ability to do work o The potential comes from charge separation o The amount of potential energy is the same inside & outside of the cell o What is the force that’s driving all of this? DIFFUSION –high to low concentration 3 Important Ways small Molecules Cross the Plasma Membrane Diffusion (O2, CO2, for ex.) Facilitated diffusion (glucose, H2O, for ex.) Active transport (Na+, K+, Ca2+) Ionic Forces Underlying Electrical Signaling in Neurons (chemical & electrical) 1. Diffusion (chemical force) a. Particles move from areas of high concentration to areas of low concentration (aka they move down their concentration gradient) 2. Diffusion thru semipermeable membranes a. Cell membranes permit some substances to pass thru but not others 3. Electrostatic Forces (electrical force) a. Like charges repel, opposites attract b. Charge separation voltage (potential) **watch these animations http://2e.mindsmachine.com/av03.03.html CrashCourse video on Action Potentials! Presynaptic cell has a signal to send – will reach the dendrites of another (post-synaptic) neuron o Communication bw them is synaptic transmission (bw neuron 1 & cell body of neuron 2) –signal is inhibitory or excitatory o generation of local graded potential @post-synaptic terminal o transfer bw pre-synaptic to post-synaptic—chemical o local graded potential travels around membrane—THEN when it reaches axon hillock it’s either all or nothing! Resting membrane potential voltage: -60mV IPSP: voltage gets more negative-hyperpolarization EPSP: voltage gets more positive- depolarization o pre-synaptic voltage-dependent calcium channel –will open only when a certain level of voltage is reached ! o calcium reaches pre-synaptic membrane, fuses w/it (exocytosis), then releases neurotransmitters in the synaptic cleft o then in neuron 2, @axon hillock, an AP is generated (electrical) IF voltage reaches o neurotransmitters (ex. Acetylcholine-inhibitory or excitatory, dopamine-excitatory, GABA-inhibitory) any neuron only contains one type of neurotransmitter – determines if EPSP or IPSP if you have a nt, that comes from an excitatory cell, what kind of response will happen in post-synaptic? EPSP GABA (amino acid), for ex., creates an IPSP in post- synaptic terminal bc it’s inhibitory The most abundant & inhibitory NTs are amino acids (ex. Glutamate & GABA) o ligands o in post-synaptic membrane, @some synapses there are ionotropic receptors (aka ligand-gated channels) DA, for ex., binds to ligand-receptor Agonists mimic ligand/neurotransmitter/drug –binds as DA would Antagonists block the receptor channels by binding to it and not letting other NTs bind o A given NT may interact w/many different receptors in different parts of the brain o cell’s response to agonist (mimics ligand exactly) down- regulation o cell’s response to antagonist (blocks receptor) up-regulation – make more or less receptors? 2 types of receptors in post-synaptic membrane o ionotropic (fast)- channel is normally closed, but when a ligand binds to it, the receptor channel changes in shape/ opens only ions go thru & enter cell o metabotropic (slow-bc there’s an extra step): NT binds tond G-protein-coupled receptor, but there’s a G-protein (2 messenger) activated, G-protein goes to neighbor ion channel & opens it IN THE MEMBRANE (before axon hillock): ATPase pump o Passive channels: K+, Na+, ATPase sodium/potassium pump (active transport), all the receptors Threshold: -40mV IN AXON: 2 types of voltage-dependent channels (K+ or Na+) , & K+/Na+ pump o Helps info relay very quickly A CELL AT REST: Resting potential : -60mV o @resting, cell’s interior is more negative than the exterior o most Na+, Cl-, & Ca2+ are outside o most K+ ions & negatively charged proteins are inside the neuron o sodium-potassium pump (requires energy): pushes Na+ out & pulls K+ ions in: for every 2 potassium ions pumped into the cell, 3 sodium (Na+) are pumped out o membrane is selectively permeable to K+ but not Na+ K+ can flow to outside, down their concentration gradientinside is more negative hyperpolarization: inside of neuron becomes more negative (IPSP)— decreases chance of an AP firing 9 o IPSPs often result from Cl- channels opening, which means they rush into the cell & make it more negative depolarization: inside of neuron becomes more positive (EPSP) whether a neuron fires an AP is determined by the balance in excitatory & inhibitory signals it’s receiving, & it receives both types at all times local potential: an electrical potential initiated by stimulation at a specific site, that spreads passively along the cell membrane, decreasing in strength w/time & distance. By the time it gets to axon hillock, we’ll see if the voltage meets the threshold for an AP to fire! Threshold for AP to fire: action potential: a spike in voltage (+40mV), reversing the membrane potential momentarily, making the inside of the membrane more + than outside o Makes sense, since an AP is created by the sudden movement of Na+ ions into the axon o This shift is made possible by voltage-gated Na+ channel, bc if the voltage reaches threshold, the channel opens to allow Na+ ions thru o Na+ channels close after about 1ms, and by this time the membrane potential has shot up to ~+40mV. o K+ ions are pushed out, helped by the opening of additional voltage-gated K+ channels K+ rushes out & resting potential is restored! If too many K+ rush out, cell is hyperpolarized (gets even more negative than resting potential) Unlike graded potential, action potential is actively propagated down the axon All-or-none property: either an AP fires @full amplitude or does not fire at all o Stronger stimuli= higher frequency of action potentials produced, but not stronger APs Now how does the AP travel? It’s regenerated along the length of the axon –each segment is depolarized one after the other o each adjacent axon segment is also covered w/voltage-gated Na+ channels, the depolarization immediately creates law of dynamic polarization: axon conducts APs in only 1 direction- from axon hillock to axon terminals conduction velocity varies o larger axons: depolarization spreads faster thru interior o myelin sheath (created by glial cells) facilitates much faster AP conduction & does not let anything leak out of the cell interrupted by nodes of ranvier—AP jumps from node to node (salutatory conduction) along axon MS (multiple-sclerosis) is characterized by the degeneration of myelin –without myelin, messages are not efficiently sent down the axon or to other neurons When an AP reaches the end of an axon, it causes the axon to release a chemical (neurotransmitter) into the synapse o When an axon releases NT’s into a synapse, they briefly change the membrane potential of the other cell (changes are called postsynaptic potentials) Synaptic cleft: space bw pre-and postsynaptic membranes Synapses Convert Electrical Signals into Chemical Signals o In response to the arrival of an AP, there is an influx of Ca+ ions into the axon terminal o This calcium influx causes synaptic vesicles to rupture & release transmitter molecules into the synaptic cleft o NTs bind to postsynaptic receptors, i.e. EPSPs or IPSPs are created Dendrites vs. Axons o Axons are thin & uniform, just 1 per neuron, info flows away from cell body o Dendrites are thick & variable, many per neuron, info flows INTO cell body Intracellular (inside cell) is negative (polarized) Extracellular (outside cell) is positive o Membrane of the cell is made of phospholipids (phospholipid bilayer-fat) Size: Big things (such as a protein) can’t cross the membrane—only small stuff can cross the membrane –-lipid bilayer is impermeable to charged ions & to big ions o Based on their electrical properties When it’s unchargedcan cross easily –diffusion Other way to cross membrane—lipids open channels – facilitated transport It ions are lipophobiccannot cross If ions are hydrophilic ACTIVE TRANSPORT: go against the concentration gradient (low to high)—requires ATP (energy) Active transport is the role of the sodium potassium pump Diffusion force: high to low concentration—no energy required! Resting membrane potential: -60 mV o A lot of sodium outside the cell, lots of K+ inside the cell o Permeability= conductance o Inside K+ (150) Na+ (15) Cl- (10) o Outside K+ (5) Na+ (150) Cl- (110) o K+ can use facilitated transport to go from high to low concentration –goes out of the cell then the interior is more negative K+ goes in & out- can’t decide where to be (attracted to negative charge)—@some point, there is equilibrium outside vs. inside of cell With the electrical gradient, K+ goes from positive (outside) to negative back to inside o Na+ goes from outside to inside o Cl- goes from outside to inside NERNST EQUATION o Nernst equation is the first to look at the membrane potential, but only addresses equilibrium for one ion at a time o Individually cannot explain each voltage o GOLDMAN EQUATION –tried to explain -60mV, the resting membrane potential o What Nernst didn’t take into account was the distribution of each ion channel o Used the permeability of the membrane for each ion to explain the resting membrane potential o Cell has a lot of K+ channels, few for Na+ & Cl- LAB 3 NOTES Neurons receive 2 types of local graded potentials (messages) Excitatory (EPSPs): resting membrane potential becomes more positive Inhibitory (IPSPs): resting membrane potential becomes more negative Action potentials transmit messages by moving down the axon (electrical) create neurotransmitters to translate message to next neuron in synaptic space (chemical) Local graded potentials always hit resistence as they move along the axon & lose energy/get weaker message goes slower and/or for shorter distance Spatial Summation: different voltage amounts from different messages at the dendrite add together Temporal Summation: ifLGPs arrive at the same time & they cancel each other out Switch from 100K (Ri) to 30K (Ri)= less resistance o 100K has higher internal resistance (Ri) o How can we get lower Ri? fatter dendrite The lower the Rm is, the shorter the length constant o If Rm is very high, nothing can leak out/ions stay inside longer length constant (traveling distance) o How do we get a higher Rm? myeline sheath The lower Ri (internal resistence), the longer the length constant (traveling distance) inside Convergence: synaptic integration o Excitatory neural transmission: INCREASED probability of an action potential (EPSP) o Inhibitory neural transmission: DECREASED probability of an action potential (IPSP) Divergence: amplification o 5 different signals are converging @these dendrites – plus-sign ones are excitatory (red) o if it depolarizes enough, at the axon hillock an AP will generate & will propagate down the axon o (middle photo): if the inhibitory neurons are at the same time as excitatory neurons that push n pull can generate info in the brain only a small # of cells are able to fire- how? The inhibition might be less for that cell for a fraction of a second, or maybe the excitation is strong/plenty enough to fire an AP If the next neuron doesn’t generate an AP, that signal is lost Prof’s Summary: presynaptic- neurotransmitter release postsynaptic- receptor binding ion channels open ionic current flows across membrane postsynaptic membrane potential changes (graded, decrementing PSP) postsynaptic cell is excited or inhibited (IPSP or EPSP) summation of PSP determines if an AP is triggered Short-Term (last less than a second) in Chemical Synaptic Transmission ~ “Plasticity” rapid stimulation- tetanus the nervous system isn’t fixed- activity across the synapses change the functions Short-term plasticity mechanisms- Facilitation depolarization AP o 2 ndAP comes, there’s still residual calciumtriggers another AP o more Ca+ available more responses o calcium pump has to pump calcium out (requires energy) o but before it pumps it all out, next AP comes aka facilitation! Depression o The neurotransmitter is being released from the cell –receptors are not responding to the neurotransmitters bc there are no more n These synapses are dynamic thru their use—changing their function Chemical Neurotransmission (in a cell at rest) Ionotropic Receptors (ion-feeding) o When a nt binds it, it makes a hole in the membrane positive ions can enter the cell o The driving force of sodium is about 6x greater o When cation channel opensmore depolarization Metabotropic Receptors – there are tons of different kinds o The G-protein itself changes shape, dissociates from receptor, moves in the membrane, releases another metabolite ion channel opens –for sodium OR potassium the receptor & its properties determine what the response will be in the post-synaptic cell the receptor ‘designs the cell’s response’ the receptor is a protein, a product of the genome Ligands (neurotransmitters): the thing that binds to another thing agonist drugs: mimic an andogenous neurotransmitter or ligand— causes that receptor to do more of what that receptor does antagonist drugs: interferes w/what that receptor would do by blocking it o can be competitive or non-competitive the cells are not passive – cells can change their sensitivity to drugs by changing the # of receptors they make in response to ‘experience’ o cell’s response to agonist (mimics ligand exactly) down- regulation o cell’s response to antagonist (blocks receptor) up-regulation – make more or less receptors? 2 types of receptors in post-synaptic membrane o ionotropic (fast)- channel is normally closed, but when a ligand binds to it, the receptor channel changes in shape/ opens only ions go thru & enter cell o metabotropind(slow): NT binds to receptor, but there’s a G- protein (2 messenger) activated, G-protein goes to neighbor ion channel & opens it Lecture 8 (Kally): Development of the Brain! \ Neural systems develop according to a genetic program that is refined by neuron-specific experience Neuroplasticity: ability of the nervous system to change in response to experience or environment HoW? o Make a lot of neurons o Tell them where to go o Tell them what type of neuron to be o Connect them to each other o Organize their functions Group them into function Refine that w/experience What drives patterning? –gene expression What guides development? -organizer regions 1. PROLIFERATION: radial glia guide migrating cells a. Cell differentiates into a neuron cell continues to undergo mitosis 2. MIGRATION: radian glia guide migrating cells a. Inside out migration of neurons b. Sister cells split up & part ways 3. DIFFERENTIATION: what types of neuron will they be? a. How is cell fate determined? -by location & the signals around that location, as well as what they are exposed to! b. Your fertilized egg divides into 2, then into 4, into 8, so on until you have about 100 cells –looks like a ball w/a hollow center (frog blastula-stage—v early stage) c. d. how is differentiation regulated? - by molecules in the local environment 4. SYNAPTOGENESIS (connect the cells to each other) a. Neurons have filopodia (little feet) b. Axon finding & fine tuning c. Pruning & cell survival i. We’re born w/2x as many neurons & connections as we’ll have as adults ii. Brain volume doubles over the 1 2 years of our lives d. APOPTOSIS (programmed cell-death) i. 3 signals: die, don’t die, die! --regulated by death genes ii. planned way to get rid of cells we don’t need iii. how is our brain still increasing in size then? 1. Myelination—adds a lot of volume 2. Inhibitory neurons grow & make connections a little later 5. Organize their functions! --defined by intrinsic interactions a. If you change the gradients, the cortex changes in size b. Experience is key! (mainly for pruning 6. PLAN a. Timing is so important --- ‘critical periods’
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